STAT蛋白
贾纳斯激酶
JAK-STAT信号通路
信号转导
医学
急性胰腺炎
斯达
磷酸化
Janus激酶2
细胞因子
车站3
白细胞介素6
癌症研究
内科学
药理学
细胞生物学
生物
酪氨酸激酶
作者
Jianxia Dong,Xiaohong Chen,Yi Song,Xiaofan Fei
出处
期刊:PubMed
[National Institutes of Health]
日期:2019-04-01
卷期号:39 (2): 166-173
被引量:4
摘要
To investigate the effect of Chaiqin Chengqi decoction (CQCQD) on acute pancreatitis (AP) by janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway in vitro and in vivo.AP was induced by caerulein both in AR42J cells and in mice. AR42J cells were divided into five groups: the control group, the AP group, the CQCQD group, JAK/STAT signaling pathway inhibitor AG490 group, and the CQCQD and AG490 group. After induction, cellular supernatant of five groups were collected for measuring the concentrations of inflammatory cytokine amylase, interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), nuclear factor κB (NF-κB) by enzyme-linked immunosorbent assay and the expression of JAK-2, STAT-3 signaling transduction proteins by Western blot, respectively. Experiments in mice were performed similar to that of in AR42J cells.Treatment of AR42J cells with CQCQD reduced the pancreatic injury and negatively regulated the activities of amylase, as well as inhibited expression of several inflammatory cytokines such as IL-6, TNF-α, IL-1β, NF-κB. Administration of CQCQD significantly inhibited JAK-2 activation and down-regulated phosphorylation of downstream substrate STAT-3 the same as AG490, resulting in inhibition of inflammatory mediators and amelioration of pancreatitis.The results suggested that CQCQD exerted anti-inflammatory effects on AP via reducing expression and phosphorylation of JAK and STAT.
科研通智能强力驱动
Strongly Powered by AbleSci AI